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Journal Article

Effect of N-Acetyl Cysteine on Oxidative DNA Damage and the Frequency of DNA Deletions in Atm-Deficient Mice

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http://pubman.mpdl.mpg.de/cone/persons/resource/persons83912

Fischer,  E
Department Human Perception, Cognition and Action, Max Planck Institute for Biological Cybernetics, Max Planck Society;
Department Physiology of Cognitive Processes, Max Planck Institute for Biological Cybernetics, Max Planck Society;

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Schiestl, R., Fischer, E., & Reliene, R. (2004). Effect of N-Acetyl Cysteine on Oxidative DNA Damage and the Frequency of DNA Deletions in Atm-Deficient Mice. Cancer Research, 64, 5-5. Retrieved from http://cancerres.aacrjournals.org/cgi/content/full/64/15/5148.


Cite as: http://hdl.handle.net/11858/00-001M-0000-0013-D801-F
Abstract
Ataxia telangiectasia (AT) is a hereditary human disorder resulting in a wide variety of clinical manifestations, including progressive neurodegeneration, immunodeficiency, and high incidence of lymphoid tumors. Cells from patients with AT show genetic instability, hypersensitivity to radiation, and a continuous state of oxidative stress. Oxidative stress and genetic instability, including DNA deletions, are involved in carcinogenesis. We examined the effect of dietary supplementation with the thiol-containing antioxidant N-acetyl-L-cysteine (NAC) on levels of oxidative DNA damage and the frequency of DNA deletions in Atm-deficient (AT-mutated) mice. We confirmed that Atm-deficient mice display an increased frequency of DNA deletions (Bishop et al., Cancer Res 2000;60:395). Furthermore, we found that Atm-deficient mice have significantly increased levels of 8-OH deoxyguanosine, an indication of oxidative DNA damage. Dietary supplementation with NAC significantly reduced 8-OH deoxyguanosine level and the frequ ency of DNA deletions in Atm-deficient mice. These levels were similar to the levels in wild-type mice. Our findings demonstrate that NAC counteracts genetic instability and suggest that genetic instability may be a consequence of oxidative stress in Atm-deficient mice.